Experimental models of graft arteriosclerosis.

Behzad Soleimani, Victor C. Shi

Research output: Contribution to journalReview article

4 Citations (Scopus)

Abstract

Graft arteriosclerosis (GA) is the leading cause of mortality in long-term survivors of solid organ transplantation. Although clinical studies have suggested a multifactorial etiology, the precise mechanism of disease remains obscure. Many animal models have been developed that manifest lesions resembling those of human arteriosclerosis. These models have helped us address specific mechanistic and interventional issues but, for reasons that will be discussed, have failed to assign a unitary pathogenic mechanism to clinical GA. In this chapter we describe the commonly available experimental models of GA. We further discuss the merits and limitations of each model and outline their contribution to our understanding of the pathogenesis of the disease.

Original languageEnglish (US)
Pages (from-to)401-424
Number of pages24
JournalMethods in molecular biology (Clifton, N.J.)
Volume333
StatePublished - Jan 1 2006

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Arteriosclerosis
Theoretical Models
Transplants
Organ Transplantation
Survivors
Animal Models
Mortality

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Genetics

Cite this

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Experimental models of graft arteriosclerosis. / Soleimani, Behzad; Shi, Victor C.

In: Methods in molecular biology (Clifton, N.J.), Vol. 333, 01.01.2006, p. 401-424.

Research output: Contribution to journalReview article

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AU - Soleimani, Behzad

AU - Shi, Victor C.

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N2 - Graft arteriosclerosis (GA) is the leading cause of mortality in long-term survivors of solid organ transplantation. Although clinical studies have suggested a multifactorial etiology, the precise mechanism of disease remains obscure. Many animal models have been developed that manifest lesions resembling those of human arteriosclerosis. These models have helped us address specific mechanistic and interventional issues but, for reasons that will be discussed, have failed to assign a unitary pathogenic mechanism to clinical GA. In this chapter we describe the commonly available experimental models of GA. We further discuss the merits and limitations of each model and outline their contribution to our understanding of the pathogenesis of the disease.

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